Chronic kidney disease (CKD) affects 1 in 10 American adults and its prevalence is rapidly increasing. In the United States alone, 90,000 patients will die from end stage renal disease (ESRD) each year, and over $40 billion is spent on treatment of CKD and ESRD. While most of the burden of CKD is focused on ESRD, even the mild stages of CKD are not benign and result in both higher risks of cardiovascular disease and increased health care costs.
Glomeruli, the functioning structure of nephrons, can lose their function due to high blood pressure, disease affecting the kidney, and other attributes of health. It is now well known that lower number of functioning nephrons are associated with higher susceptibility to kidney disease and hypertension. A low number or a loss of nephrons leads to glomerular hypertrophy and hyperfiltration. The theory behind this is that a kidney with a low number of nephrons must filter the same amount of fluid per unit time as a kidney with high nephron number, and therefore to maintain an acceptable total filtration surface area and a constant glomerular filtration rate (GFR), each glomerulus in a poorly endowed kidney must grow larger and filter more fluid than its healthy counterpart. While this likely compensatory mechanism may maintain homeostasis in the early stages, it complicates the use of GFR measurements for early detection of kidney diseases involving changes in nephron number and glomerular volume. Ideally, clinical measurements of glomerular number and volume can be used to detect and monitor loss of nephrons and glomerular hypertrophy in patients at risk of CKD, such as those with diabetes and hypertension.
Currently, measurements of total nephron number (Nglom) and mean glomerular volume (Vglom) require histological sectioning and quantitation of a fraction of a kidney and extrapolation to a total glomerular number and volume. Studies employing these methods have provided significant insights into renal physiology and the role of Nom, and Vglom in both kidney-specific and systemic diseases. Unfortunately, these methods require resection and destruction of the kidney. At this time, there are no methods available for direct measurements of Nglom, Vglom, or protein leakage of individual glomeruli in vivo. Such methods would provide a window for early intervention and may also prove vital in assessing renal allograft viability prior to transplant.
Therefore, it would be desirable to have a system and method for detecting and monitoring kidney function capacity noninvasively and at early stages.